Mechanisms underlying short-term synaptic plasticity between identified neurons

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All nervous system functions rely upon neuronal communications through specialized structure, termed synapse. Diffusion of electrical activity-induced, neurotransmitters across the synaptic cleft and its activation of juxtaposed receptors on the recipient cell enable the flow of information across all brain circuits. Failure of this neuronal communication renders the brain dysfunctional. Despite extensive research in the field of neuroscience, the precise cellular and molecular mechanisms that regulate various modes of synaptic communications remain, however, largely unknown. Moreover, even less is known about the mechanisms that enable neurons to either increase or decrease their synaptic strength (synaptic plasticity) in response to a changing environment. We have developed a simple model comprising of functionally defined neurons from the snail. This model has not only allowed us to define mechanisms underlying synaptic transmission, but has also helped design silicon chips that can be interfaced with brain cells. Using this model, we will now define both cellular and molecular pathways that regulate not only the synaptic transmission, but also the short-term synaptic plasticity that forms the basis for learning and memory. Neuronal networks will be reconstructed in cell culture and using several state-of-the-art neuroscience techniques, we will identify mechanisms that regulate neuronal communication under normal conditions and after short-term synaptic plasticity that form the basis for learning and memory. We will seek to determine how calcium entry into neurons activates a cascade of second messengers that in turn affect neuronal output during working memory.